Reduced glial density and neuronal volume in major depressive disorder and schizophrenia in the anterior cingulate cortex

Cotter, David; Mackay, Daniel; Beasley, C.; Kerwin, Robert; Everall, Ian

doi:10.1016/s0920-9964(00)90552-8

Cited by 15 publications

(5 citation statements)

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“…Post-mortem morphometric studies revealed that the marked deficit of total glial population is one of the most consistent findings in the prefrontal cortex (PFC) (Cotter et al, 2002;Stark et al, 2004) in SZ. A similar deficit of glial cells was also found in the PFC in mood disorders (Cotter et al, 2001;Ongur et al, 1998;Rajkowska et al, 2001). There are only few electron microscopic qualitative studies that demonstrated alterations of myelinated fibres and oligodendrocytes in SZ (Miyakawa et al, 1972;Senitz and Winkelman, 1981;Uranova and Orlovskaya, 1996).…”

Section: Introductionmentioning

confidence: 56%

The role of oligodendrocyte pathology in schizophrenia

Vostrikov

Vikhreva

et al. 2007

Int. J. Neuropsychopharm.

155

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Neuroimaging and microarray studies provide evidence for myelin and oligodendrocyte abnormalities in schizophrenia (SZ). Electron microscopy demonstrated dystrophy, necrosis and apoptosis of oligodendrocytes, the most severely affected cells in SZ. The proportion of myelinated fibres with atrophy of axon and swelling of periaxonal oligodendrocyte processes increased significantly in the prefrontal cortex (PFC), caudate nucleus and hippocampus in SZ compared to controls. Morphometry showed a deficit of oligodendrocytes in the PFC and in adjacent white matter, lower number of oligodendroglial satellites of pyramidal neurons and a loss of pericapillar oligodendrocytes in the PFC in SZ compared to normal controls. A lowered number of oligodendrocytes in the PFC was also found in mood disorders. These data provide evidence for altered oligodendrocyte-axon, oligodendrocyte-neuron and oligodendrocyte-capillar interactions in SZ brains suggesting a key role of damage and loss of oligodendrocytes in altered neuronal connectivity and in atrophy of neurons in SZ.

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Section: Introductionmentioning

confidence: 56%

The role of oligodendrocyte pathology in schizophrenia

Vostrikov

Vikhreva

et al. 2007

Int. J. Neuropsychopharm.

155

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“…During effective antidepressant, treatment, most PET studies have shown that pregenual ACC flow and metabolism decrease in posttreatment scans relative to pretreatment scans. 1 The finding that this region contains histopathological changes in MDD and BD 20 , 64 , 68 suggests the hypothesis that, the abnormal reduction in metabolism in treatment-nonresponsive cases reflects more severe reductions in cortex.…”

Section: Implications For the Pathogenesis Of Emotion Dysregulationmentioning

confidence: 98%

“… 7 , 9 , 18 , 55 The histopathological correlates of these abnormalities included reductions in glial cells with no equivalent loss of neurons, reductions in synapses or synaptic proteins, elevations in neuronal density, and reductions in neuronal size. 9 , 17 , 18 , 20 , 40 , 64 , 65 Abnormal reductions in glial cell counts and density, and/or glia-to-neuron ratios have also been found in MDD in Brodmann area (BA) 24 cortex of the pregenual ACC, 20 the dorsal anterolateral PFC (BA9), 21 , 66 and the amygdala. 1 , 67 Finally, the mean size of neurons was reduced in the dorsal anterolateral PFC (BA9) in M'DD subjects relative to controls, 18 and the density of neurons was decreased in the ACC in BD.…”

Section: Postmortem Neuropathological Assessments Of Mood Disordersmentioning

confidence: 99%

Neuroplasticity in mood disorders

Drevets¹

2004

Dialogues in Clinical Neuroscience

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Neuroimaging and neuropathological studies of major depressive disorder (MDD) and bipolar disorder (BD) have identified abnormalities of brain structure in areas of the prefrontal cortex, amygdala, striatum, hippocampus, parahippocampal gyrus, and raphe nucleus. These structural imaging abnormalities persist across illness episodes, and preliminary evidence suggests they may in some cases arise prior to the onset of depressive episodes in subjects at high familial risk for MDD. In other cases, the magnitude of abnormality is reportedly correlated with time spent depressed. Postmortem histopathological studies of these regions have shown abnormal reductions of synaptic markers and glial cells, and, in rare cases, reductions in neurons in MDD and BD. Many of the regions affected by these structural abnormalities show increased glucose metabolism during depressive episodes. Because the glucose metabolic signal is dominated by glutamatergic transmission, these data support other evidence that excitatory amino acid transmission is elevated in limbic-cortical-striatal-pallidal-thalamic circuits during depression. Some of the subject samples in which these metabolic abnormalities have been demonstrated were also shown to manifest abnormally elevated stressed plasma cortisol levels. The co-occurrence of increased glutamatergic transmission and Cortisol hypersecretion raises the possibility that the gray matter volumetric reductions in these depressed subjects are partly accounted for by processes homologous to the dendritic atrophy induced by chronic stress in adult rodents, which depends upon interactions between elevated glucocorticoid secretion and N-meihyl-D-aspartate (NMDA)-glutamate receptor stimulation. Some mood-stabilizing and antidepressant drugs that exert neurotrophic effects in rodents appear to reverse or attenuate the gray matter volume abnormalities in humans with mood disorders. These neurotrophic effects may be integrally related to the therapeutic effects of such agents, because the regions affected by structural abnormalities in mood disorders are known to play major roles in modulating the endocrine, autonomic, behavioral, and emotional experiential responses to stressors.

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“…The Drevets' group findings, spanning PET, MRI and histological data, are intriguing, but it would be premature to accept a loss of glia from the cingulate cortex as the first unequivocal neuropathological abnormality of mood disorder until there is independent replication. The closest yet reported is by Cotter et al, 12 who examined a different part of the anterior cingulate gyrus from the same brain series -the Stanley Foundation brain bank collection. 13 They confirmed a decreased glial density in major depression, but not in bipolar depression; they also found a glial reduction in schizophrenia.There are preliminary reports of other aspects of glial pathology in the prefrontal cortex in these mood disorder subjects.…”

Section: Anterior Cingulate Cortexmentioning

confidence: 99%

Neuropathological studies of bipolar disorder

Harrison

2000

Acta Neuropsychiatr.

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The few available neuropathological studies of bipolar disorder are reviewed and placed in the context of structural imaging findings. Candidate pathological processes include cy-toarchitectural abnormalities, particularly in the anterior cingulate cortex and affecting glia, and disruption of white matter connections. The possible neuropathological relationship of bipolar disorder with major depression and with schizophrenia is discussed.

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Reduced glial density and neuronal volume in major depressive disorder and schizophrenia in the anterior cingulate cortex

Cited by 15 publications

References 0 publications

The role of oligodendrocyte pathology in schizophrenia

The role of oligodendrocyte pathology in schizophrenia

Neuroplasticity in mood disorders

Neuropathological studies of bipolar disorder

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